Manna from Chemtrails: From Amyloids to Nanoids

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This is the first in a series of articles on Alzheimer’s Disease and the amyloid catalysts that have stalked humanity for quite some time will be presented. The series will also examine Morgellons Syndrome – a cousin of Alzheimer’s.

Manna from chemtrails has many vectors within its gases and liquid composition. The use of smart dust, to appear as space dust, smart meters to measure the smart dust particles, and the NERC grid to control the particles, then we are looking at another form of electrical control of the planet. Aromatic hydrocarbons can be manufactured. Frequencies can be altered. Is it amyloid that forms the fibers that can be formed into light encoded strands? Has a secondary system connected to particles been created to control the expression of our DNA?

“I know a world midway in size between the Moon and Mars,” said Carl Sagan, “where the upper air is crackling with electricity; where the perpetual brown overcast is tinged an odd burnt orange; and where the stuff of life falls out of the skies like manna from heaven onto the unknown surface below.”

And what is that “stuff of life” that Sagan is talking about?  That “manna from heaven”?

Hydrocarbons and nitriles constantly fall from Titan’s skies, said Sagan. Titan – the big moon of Saturn – is socked in as a haze of organic solids formed high in its skies slowly fall and accumulate on its surface. Oceans of water are impossible on Titan (it’s too cold), but “vast oceans of liquid hydrocarbons are expected.”

http://www.evolutionaryleaps.com/Excerpts.htm

Alzheimer’s is an extension of the Amyloidosis diseases. Alzheimers was around before Alois Alzheimer’s successors had given this disease his name. Indications of this type disease were apparent back in Roman times. One can see that after some research that amyloid seems to be at the center of these afflictions. The following overview is a good wrap around this mysterious amyloid, which is just as mysterious as both Alzheimers and Morgellons. It was a scientist from 1838 that set my focus onto the core of amyloids. There are now 23 proteins that can form fibrils. At the time of the following report, there were 20, so the number of amyloid forming fibrils is increasing.

“Amyloids are insoluble proteins formed as a result of errors of intra molecular self-assembly and it forms the contributory component of many of degenerative diseases. The word amyloid was coined by Matthias Schleiden, a German botanist in 1838 to describe a normal amylaceous constituent in plants… However, Virchow used the word first in the medical field to describe some small round deposits in the nervous system in 1854. So far twenty different unrelated proteins were identified to be the amyloid precursors and are capable of forming stable amyloid fibrils …”   See:

http://www.pharmainfo.net/reviews/amyloids-and-amyloidosis-overview-mis-folded-proteins-and-their-diseases

Morgellons, an extension of Alzheimer’s, found in other areas of the human body, not just in the brain, include different replicators. At the core of Amyloidosis, Sclerosis, Sarcoidosis, Alzheimer’s and Morgellons which I call the (ASSAM) group is the amylaceous material which is a carbohydrate/starchy sugar/calcium component. Downs Syndrome (by the age of 35 often get Alzheimers), Hodgkins, Parkinsons Arterial sclerosis, Atherosclerosis, Rheumatoid Arthritis, Mitochondria diseases, Multiple Myelomas, Monoclonal, Pancreas diseases and Diabetes are now related to amyloid and heavy/light chain alterations.

There are other diseases now surfacing including scoliosis, dystrophies and sympathies, affecting the muscles as well, including the heart. These possibly have the same core as the ASSAM group, but, with different, modifications and different reactions. I will attempt to walk through the process of amyloid formations, the new forms I call nanoids and how these forms have altered the landscape of the human body terrain.

Amylaceous matter is starchy material. See:
http://www.wordnik.com/words/amylaceous

This sugar starchy component is either a succinyl or a mannose, in the form of oligosaccharide, octasaccharide or polysaccharide. It has been shown in the literature on Alzheimer’s that oligomers form fibrils or tau. These are formed from the amyloid depositions. The amyloid precursor protein (APP) is an alpha- beta crystallin form. It reacts to hydroxyl radicals and calcium. The RNA polymerase genome is used as a vector. The Amyloidal Precursor Protein is the core of this disease and all of the amyloidal diseases. Morgellons is the actual initiation of these oligomers as RNA polymerase.

Below, is a reference on a study of prions, the RNA involvement, and oligomers as polymers. Nano materials weigh heavily as well as amphiphiles used in the formation of Morgellons manifestations. Since then, bolaamphihiles, which have few if any artifacts are used. This is a new form of not only weeding out individuals, but, for increasing the strength of certain types who can benefit from artificial integration of the super molecular cells. Differentiation due to phenotypes and genotypes will determine whether one lives or dies of one of the amyloid diseases, including the new syndrome, Morgellons.

In Alzheimer's disease, changes in tau protein lead to the disintegration of microtubules in brain cells.

(For more details on the above image, see “Biochemistry” section on the Alzheimer’s disease wiki

Research is now involved in searching for the core of the amyloid and it has been suggested that oligomers especially PrpC-RNA oligomers, may cause the neurotoxicity. In Morgellons the oligomers are insoluable, so the initiation was altered to include the amphiphiles and the bolaamphiphiles. This is a program initiatied and kept behind doors of UNESCO. However, the finding that prions are related to the oligomers is now evident.

The researchers claim that: “The formation and aggregation of PrpSC has been the commonly accepted cause for Prion disease. However, Mellucci et al showed PrpSC may not be contributing to neurotoxicity as PrpC depletion can reverse early Prion disease stage despite PrpSC replication in vitro . Another study characterized PrpC -oligomers in Scrapie-infected brain (4). Therefore, it is suggested that an intermediate form, possibly the soluble, protease sensitive PrpC-RNA oligomers, may be the initiators to neurotoxicity…” See: http://tinyurl.com/6bc6h5g

The oligomers are considered the culprit of the neurodegenerative process associated to AD, although the pathogenic mechanism activated by these small aggregates remain to be elucidated. In the initial study based on the binding screening PrPc was identified as ligand /receptor of A? oligomers, while long term potentiation (LTP) analysis in vitro and behavioral studies in vivo, demonstrated that the absence of PrPc abolished the damage induced by A? oligomers. The high affinity binding A? oligomers-PrPc has been confirmed, whereas a functional role of this association has been excluded by three different studies. We approached this issue by the direct application of A? oligomers in the brain followed by the behavioural examination of memory deficits. Our data using PrP knock-out mice suggest that A? 1-42 oligomers are responsible for cognitive impairment in AD but PrPc is not required for their effect.  See:

http://www.landesbioscience.com/journals/22/article/14367/

However, other prion types, especially those formed from the sup35protein and sup45 proteins are producing many amyloid diseases. These have heat shock proteins from archaea and other organisms in them. These not only form fibrils, they form prions, which unfold the protein. They also form fibers and fibrils, of different sizes. These prions are from genes taken from Podospora Ansinera and the memory genes from California Aplysia, a slug. So, other than the CJD diseases and Scrapie, BSE and TSE, these form other types of prions.

A consistent amount of prions are formed to unfold proteins and fold in the oligomers. They are most likely used as vector, as is the virus, both known to be not live, but once inside the cell, become a live entity. It is what they carry that causes the damage. One of the main causes of amyloid deposition is the Abeta 42 crystallin made of starchy sugar resins. This starchy sugar causes the amyloidal spherules. This is a strong statement to make, but all of the amyloidal diseases are involved in this formation of these particles or canaluculi.   And there is evidence that calcium channels are formed from the oligomers, and that calcium helps form the initiation of the growth of the oligomers by way of the Abeta protein. An image from a study examining the abeta oligomers and the calcium channels they form is shown here:

Calcium channels created by amyloid beta oligomers

“Small molecule blockers of the Alzheimer A? calcium channel potently protect neurons from A? cytotoxicity” by Juan Carlos Diaz, Olga Simakova, Kenneth A. Jacobson, Nelson Arispe, and Harvey B. Pollard.  See “Preventing neurotoxicity in Alzheimer’s disease”

Oligomers are also involved in heavy and light chain operations in the human body. These normal chains have been altered by these polymers. An oligomer is defined as “A polymer that consists of two, three, or four monomers” as described in the OnLine Free Dictionary which also describes a monomer as: “A molecule that can combine with others to form a polymer.” The common denominator here is the polymer. Notice they are all mers. A mer is the replicator, the repeating unit. It is described as: “(organic chemistry) a combining form denoting the repeating structure unit of any high polymer.” (From answers.com).

What we have found in Morgellons, is a repeating unit, which is latent at times and then manifests itself, when the temperature is appropriate for its replicating form. This forms monomers which form Dimers (2 monomers) which then form oligomers (4 monomers) and then protofilaments (tau like filaments, 8 monomers) which form tubules which then form the bundles. The mer is the core unit. It is based on starchy sugars, mannose, such as octasaccharides and polysaccharides. These mers are in resin form. These resin forms harden forming the amyloids. This malicious sugar is from corn, and other edible products. These are also found in artificial gelatin products. These are in many foods, can create acetone, acetate, acetyl, artificial RNAs. The RNA polymerases I, II, III, and IV are non coding, artificial strands, called oligomers. These are made from these resins. One, for instance is aramid. This is described as:

“Based on earlier research by Monsanto Company and Bayer, a fiber – para-aramid – with much higher tenacity and elastic modulus was also developed in the 1960s–1970s by DuPont and Akzo Nobel, both profiting from their knowledge of rayon, polyester and nylon processing.” http://en.wikipedia.org/wiki/Aramid

However acetone itself was produced in early 1900s from Clostridium Acetylbotylicum. This resin was later grown in corn. It was called the “Weizmann Organism”. A process called ABE was able to process this into acetone, a rubber like material. The artificial RNA is made of similar amino acids. However, the starchy sugar resin is at the core of the amyloid formations. All from resin starchy sugar elements.

Here is link to what may be the source of the ASSAM group. From the amyloid to the non coding RNA as vector which has its own genome, now, and is being used as vector and replicator, whereas previously, the amylaceous starchy material formed from sugars was used. These polymers in the coding RNA can then be processed from the non coding RNA. These are artificial materials, in other words they are formed from chemicals.

Sugar in and of itself is a chemical, but, if an artificial source is used, like lignan, or resin in place of sugar a foreign material is integrated into the human genome as use for replacing amino acids, then we know that the base of the DNA architecture has been altered. This foreign material is the resin, of course it is natural, but not to the human body. When temperature and water level change, the particles change form. This main form is a pentagon, a pentraxin, while the monomer forms a hexagon.

The monomer proceeds to form into a dimer, a two monomer form. The dimer picks up two more monomers and forms the oligomer. This oligomer now with 4 monomers forms a protofibril. These fibrils then form a tubule with any number of fibrils within the form. This resin is in the intercellular spaces, it forms a signal so that outside the cell, it can direct information inside the cell, by crossing the sugar or glycerol barrier of the cell.

The membrane protein is a transmembrane, meaning it can go inside the cell and dump the RNA, which will then through reverse process since it is negative, link to positive RNA, thereby changing the RNA which will then change DNA, eventually. So the process for bringing in artificial synthetic life was through the protein the RNA and DNA, instead of normal route DNA, RNA and protein. So the new proteins created are now synthetic.

In all of the ASSAM diseases these synthetic proteins are tangled into the normal native proteins of the body. These were done for a purpose. The whole idea of Epigenetics is to perfect the system, however, this process of acetylation, bringing in foreign synthetics unnatural amino acids, the sugar base of the DNA structure was to bring in artificial life. This is done with Aspartame, and now Oligo Sugars. These only keep the artificial growing. These aromatic hydrocarbons are in flavinoids, any artificial flavored, colored, and gelatinized products.

Now just examining Alzheimer’s studies, one can also see the light chains have been altered. This is the histone modifications brought about by the chromosome alterations. This again, is all part of the Epigenetic Programming of the human system. This system runs parallel to our original DNA and becomes the main controller in the body. It controls the expression of our DNA.

Aceylation, methylation histone modification, phosphorylation and other events happen inside the body when these processes are activated for expression. These are activated by light signals. The heavy/light chains in the immunoglobins respond. When these have been altered only certain signals are accepted. These signals are at a higher frequency than the normal native RNA and DNA is.

The Mer is the replicating source of this new synthetic that is controlling the expression of DNA. There are many other syndromes and manifestation of these mers. Many people are dying of unknown causes, because the source has been hidden as has most information on any cancer, disease, or neurological disease are.

Here is an image of the process:

Overview of amyloid assembly mechanisms

(See “Overview of amyloid assembly mechanisms” in this article about amyloids.)  These amyloid liposomes make up the connection or adherence to the formation of the membrane itself.

Microtubule formation

(See section on Microtubule Formation in Chapter 22 – Cytoskeletal Structure and Function.)

Some of this may seem confusing, because it is. This has been a long road for many of us, but, when scientists are now seeing the amyloid for what it really is, and then progress is made. It may be late for Morgellons to really rise in the scientific studies, but the consequences of the use of foreign material in the human genome are now evident. We can only hope that these scientists and medical experts will be able to stop the synthetic drone of the artificial life Machine, whereby the body becomes a computer. That has been the goal all along, what it does is create a hive mind, all linked by higher technology and non natural intelligence. This article sums up what scientists are doing:

Obtaining real molecules in an artificial environment has been a long-time dream for biology engineers, and one that was not short on difficulties that had to be surpassed to achieve it. But now, scientists at the Scripps Research Institute, in La Jolla, California, managed to create such a molecule, a tiny fragment of RNA, which has the most important property of life – self-replication. Future plans include the endowment of the engineered material with the means to evolve and function, which would basically be the first steps toward creating artificial life.

“Obviously what we’re trying to do is make a biology,” says Scripps biochemist Gerald Joyce. “We’re trying to jump in at the last signpost we have back there in the early history of life.”

The chemical he and colleague Tracey Lincoln created was based on RNA because evolution theorists believe that this acid was the thing that formed the condition for the appearance of intelligent life on Earth. A major advantage that RNA has over DNA is the fact that it can catalyst chemical reactions, the kind that happen in our bodies thousands of times each second. And it’s all made possible by these small elements.

The way they obtained their chemical was by forcing RNA building blocks to mutate under observation, leaving them with more than 288 possible outcomes. By applying Darwin’s theory on the survival of the fittest on a microscopic level, the researchers then selected only those fragments that proved they could successfully replicate even in the harshest competitive environment.

However, the team urges people not to think that the chemical is alive yet. They say that, in order for that to happen, it has to mutate on its own and develop new abilities, without them being introduced in its sequencing artificially. But Joyce says that the obtained molecule has already been endowed with another property, though he will not mention it until the team publishes its results.”

http://news.softpedia.com/news/Artificial-Life-Might-Come-from-Self-Replicating-RNA-101593.shtml

In conclusion, I would like to emphasize that the amyloid has been around for a long time and because of its affiliation with the immunoglobin light chains, it has caused a multitude of amyloid diseases. These are not just DNA diseases. Some are adaptation products from artificial foods, ingredients in gmo foods, products for industrial use, artificial flavors, sugars, colors, and aromas. These resin gelatins are used in many foods now. They are not safe. They are made of chemicals the body is not used to and cannot adapt to because they are made from chemicals like the real natural product, but are not the real natural product.

The Downs link to Alzheimers is a clue, that a foreign adaptive artificial RNA was superimposed into the strands. How was this done? Why is Downs associated with Alzheimers? Other trisomies exist, mainly the one associated with Morgellons, as once indicated on the NIH website. This one is on the 1^st chromosome. Other trisomies and translocations have happened as well in the genome including 18, and 21 for example. Downs is inserted in Chromosome 21. There is another in 22, and the X has been activated.

In Part 2, I will delve into the amylaceous matters, prions, Bence Jones proteins, immunoglobin light chains, the sugars, the artificial polymers, and how they were instituted into the human body, 21^st, 22^nd and 23^rd amino acids. Part 3 will cover the nanoids, the amphiphiles the bolaamphiphiles and the quantum light encoding materials.

Kathryn A. Augustyn

Posted by Kathryn A. Augustyn on Aug 2 2011. Filed under Featured, Morgellons. You can follow any responses to this entry through the RSS 2.0. You can leave a response or trackback to this entry